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Theoretically, these findings by Dong et al. An important restriction of the paper by Dong et al. Appelman Find articles by Y. Appelman C. In addition to the higher oestradiol levels the reported higher levels of testosterone may be of interest. It is also relevant in this context to mention another much larger study from China that found, after control for age and body composition, no differences in reproductive hormone profiles in a large group of postmenopausal patients with coronary stenosis compared with controls [ 5 ]. However, it is important for postmenopausal women to try to preserve to pear phenotype as cardiovascular disease is still the major cause of death in women [ 10 ]. However, recent publications might change this view, as a recent paper by Schierbeck from Denmark demonstrated that an early start of hormone replacement therapy seems to benefit and decreases future atherosclerotic events [ 3 ]. Appelman, Email: The control group had lower WHR and lower levels of sex hormones. The sex hormone story in relation to cardiovascular disease is always good for a surprise. In men higher testosterone levels are associated with a reduced prevalence of metabolic syndrome and an elevated prevalence in women [ 9 ]. Where we assumed that increased levels of female sex hormones were protective against the development of cardiovascular disease, our colleagues Mei Dong et al.

With only one measurement reported the temporal changes in sex hormone levels are not available. So it is not unlikely that in the current study the observed higher oestrogen levels are an association with known risk factors that lead to MI rather than being causative. In their paper published in this edition of the Netherlands Heart Journal the authors describe a relation between the occurrence of a myocardial infarction MI in post-menopausal women and levels of sex hormones [ 1 ]. This story is confusing. Oestrogens induce matrix metalloproteinase which digests the fibrous cap of a plaque exposing the underlying thrombogenic collagen which is believed to be the mechanism involved in the adverse thrombotic effects of oestrogens in the presence of established atherosclerosis [ 7 ]. There are no indications that long-term administration of androgens to women, as occurs in the treatment of female-to-male transsexuals, is associated with a substantial increase of cardiovascular risk factors [ 8 ]. But in healthy postmenopausal women, higher androgen levels were associated with increased metabolic markers for the risk of coronary artery disease whereas slightly higher normal testosterone levels seem to relate to lower progression of atherosclerosis. It is also relevant in this context to mention another much larger study from China that found, after control for age and body composition, no differences in reproductive hormone profiles in a large group of postmenopausal patients with coronary stenosis compared with controls [ 5 ]. In conclusion, whether in this study the observed elevated oestrogens were instrumental in causing the infarction or epiphenomenal to an adrenal stress response and increased peripheral sex hormone conversion potential still remains to be answered. These are clearly the pears with a preserved waist size, and they were recruited at random with two controls matched for age only. In men higher testosterone levels are associated with a reduced prevalence of metabolic syndrome and an elevated prevalence in women [ 9 ]. So, although inconclusive there are indications that testosterone may contribute to the progression of atherosclerosis in general and coronary artery disease more specifically. The control group had lower WHR and lower levels of sex hormones. In addition to the higher oestradiol levels the reported higher levels of testosterone may be of interest.

However, recent publications might change this view, as a recent paper by Schierbeck from Denmark demonstrated that an early start of hormone replacement therapy seems to benefit and decreases future atherosclerotic events [ 3 ]. From an epidemiological perspective it was shown that in women there is a relation between the onset of the menopause and the risk of MI. The sex hormone story in relation to cardiovascular disease is always good for a surprise. In addition to the higher oestradiol levels the reported higher levels of testosterone may be of interest. Women with polycystic ovarian syndrome PCOS , an ovulation disorder associated with increased androgen levels, are more at risk to develop cardiovascular disease. Yet the beneficial effects of hormone replacement therapy were off set by the induction of thrombosis, likely in subjects who already had coronary artery disease [ 2 ]. They also had a lower body mass index BMI. As we know, surgical stress induces a marked and sustained increase of adrenal androgen secretion in postmenopausal women within the early days post-surgery [ 6 ]. With only one measurement reported the temporal changes in sex hormone levels are not available. An important restriction of the paper by Dong et al. So clearly the groups are very different. The control group had lower WHR and lower levels of sex hormones. In addition the cases more often had hypertension and diabetes. It is obvious they selected pears and apples. Moreover, it is well known that women with premature menopause have an earlier onset of atherosclerosis. Can we think of a possible mechanism by which it may cause MI? In their discussion the focus in literature is on the lowering of testosterone in males during stress and a lowering of oestrogens in females. In men higher testosterone levels are associated with a reduced prevalence of metabolic syndrome and an elevated prevalence in women [ 9 ]. Not only the distribution of the fat tissue is crucial, also the other risk factors should be checked and treated, especially diabetes and hypertension. They report that high levels of oestradiol and increased waist-to-hip ratio WHR are related to the occurrence of acute MI. In conclusion, whether in this study the observed elevated oestrogens were instrumental in causing the infarction or epiphenomenal to an adrenal stress response and increased peripheral sex hormone conversion potential still remains to be answered. Oestrogens induce matrix metalloproteinase which digests the fibrous cap of a plaque exposing the underlying thrombogenic collagen which is believed to be the mechanism involved in the adverse thrombotic effects of oestrogens in the presence of established atherosclerosis [ 7 ]. There are no indications that long-term administration of androgens to women, as occurs in the treatment of female-to-male transsexuals, is associated with a substantial increase of cardiovascular risk factors [ 8 ]. Where we assumed that increased levels of female sex hormones were protective against the development of cardiovascular disease, our colleagues Mei Dong et al.

They also had a lower body mass index BMI. In their paper published in this edition of the Netherlands Heart Journal the authors describe a relation between the occurrence of a myocardial infarction MI in post-menopausal women and levels of sex hormones [ 1 ]. The question is to what extent do the sex hormone levels contribute independently? Oestrogens induce matrix metalloproteinase which digests the fibrous cap of a plaque exposing the underlying thrombogenic collagen which is believed to be the mechanism involved in the adverse thrombotic effects of oestrogens in the presence of established atherosclerosis [ 7 ]. With only one measurement reported the temporal changes in sex hormone levels are not available. Lambalk 2 Y. Where we assumed that increased levels of female sex hormones were protective against the development of cardiovascular disease, our colleagues Mei Dong et al. From an epidemiological perspective it was shown that in women there is a relation between the onset of the menopause and the risk of MI. In addition to the higher oestradiol levels the reported higher levels of testosterone may be of interest. These are clearly the pears with a preserved waist size, and they were recruited at random with two controls matched for age only. So it is not unlikely that in the current study the observed higher oestrogen levels are an association with known risk factors that lead to MI rather than being causative. There are no indications that long-term administration of androgens to women, as occurs in the treatment of female-to-male transsexuals, is associated with a substantial increase of cardiovascular risk factors [ 8 ]. It is also relevant in this context to mention another much larger study from China that found, after control for age and body composition, no differences in reproductive hormone profiles in a large group of postmenopausal patients with coronary stenosis compared with controls [ 5 ]. The control group had lower WHR and lower levels of sex hormones. Appelman C. In fact, in postmenopausal women androgen secretion originates from the ovarian hilus driven by high gonadotropins and the adrenal gland driven by adrenocorticotrophic hormone and the oestrogens come from peripheral conversion of these androgens. Can we think of a possible mechanism by which it may cause MI? Women with polycystic ovarian syndrome PCOS , an ovulation disorder associated with increased androgen levels, are more at risk to develop cardiovascular disease. In men higher testosterone levels are associated with a reduced prevalence of metabolic syndrome and an elevated prevalence in women [ 9 ]. Moreover, it is well known that women with premature menopause have an earlier onset of atherosclerosis. Based on these observations studies were initiated to supply sex hormones in order to postpone the onset of atherosclerosis.

However, it is important for postmenopausal women to try to preserve to pear phenotype as cardiovascular disease is still the major cause of death in women [ 10 ]. Not only the distribution of the fat tissue is crucial, also the other risk factors should be checked and treated, especially diabetes and hypertension. To what extent the hyperandrogenism itself is mechanistic is unclear since the syndrome often comes with obesity and insulin resistance as known cardiovascular risk factors. So clearly the groups are very different. Appelman C. So, although inconclusive there are indications that testosterone may contribute to the progression of atherosclerosis in general and coronary artery disease more specifically. It is obvious they selected pears and apples. Moreover, it is well known that women with premature menopause have an earlier onset of atherosclerosis. However, recent publications might change this view, as a recent paper by Schierbeck from Denmark demonstrated that an early start of hormone replacement therapy seems to benefit and decreases future atherosclerotic events [ 3 ]. The control group had lower WHR and lower levels of sex hormones. Yet the beneficial effects of hormone replacement therapy were off set by the induction of thrombosis, likely in subjects who already had coronary artery disease [ 2 ]. They report that high levels of oestradiol and increased waist-to-hip ratio WHR are related to the occurrence of acute MI. In their paper published in this edition of the Netherlands Heart Journal the authors describe a relation between the occurrence of a myocardial infarction MI in post-menopausal women and levels of sex hormones [ 1 ]. From an epidemiological perspective it was shown that in women there is a relation between the onset of the menopause and the risk of MI. Can we think of a possible mechanism by which it may cause MI? They also had a lower body mass index BMI. With only one measurement reported the temporal changes in sex hormone levels are not available. Theoretically, these findings by Dong et al. The question is to what extent do the sex hormone levels contribute independently? So it is not unlikely that in the current study the observed higher oestrogen levels are an association with known risk factors that lead to MI rather than being causative. The sex hormone story in relation to cardiovascular disease is always good for a surprise. Appelman Find articles by Y. It has been reported that sex hormone levels are positively related to the total amount of fat tissue, with an inverse relation to sex hormone binding globulin [ 4 ].

They also had a lower body mass index BMI. To what extent the hyperandrogenism itself is mechanistic is unclear since the syndrome often comes with obesity and insulin resistance as known cardiovascular risk factors. An important restriction of the paper by Dong et al. Their fat tissue is the predominant source of oestrogens via its high aromatase potential. In addition to the higher oestradiol levels the reported higher levels of testosterone may be of interest. Appelman, Email: In fact, in postmenopausal women androgen secretion originates from the ovarian hilus driven by high gonadotropins and the adrenal gland driven by adrenocorticotrophic hormone and the oestrogens come from peripheral conversion of these androgens. The question is to what extent do the sex hormone levels contribute independently? It is also relevant in this context to mention another much larger study from China that found, after control for age and body composition, no differences in reproductive hormone profiles in a large group of postmenopausal patients with coronary stenosis compared with controls [ 5 ]. It has been reported that sex hormone levels are positively related to the total amount of fat tissue, with an inverse relation to sex hormone binding globulin [ 4 ]. In men higher testosterone levels are associated with a reduced prevalence of metabolic syndrome and an elevated prevalence in women [ 9 ]. The sex hormone story in relation to cardiovascular disease is always good for a surprise. Yet the beneficial effects of hormone replacement therapy were off set by the induction of thrombosis, likely in subjects who already had coronary artery disease [ 2 ]. So, although inconclusive there are indications that testosterone may contribute to the progression of atherosclerosis in general and coronary artery disease more specifically. Lambalk 2 Y. But let us assume that the oestradiol levels were elevated prior to the acute event. However, recent publications might change this view, as a recent paper by Schierbeck from Denmark demonstrated that an early start of hormone replacement therapy seems to benefit and decreases future atherosclerotic events [ 3 ]. From an epidemiological perspective it was shown that in women there is a relation between the onset of the menopause and the risk of MI. In their paper published in this edition of the Netherlands Heart Journal the authors describe a relation between the occurrence of a myocardial infarction MI in post-menopausal women and levels of sex hormones [ 1 ]. Can we think of a possible mechanism by which it may cause MI? This story is confusing. Oestrogens induce matrix metalloproteinase which digests the fibrous cap of a plaque exposing the underlying thrombogenic collagen which is believed to be the mechanism involved in the adverse thrombotic effects of oestrogens in the presence of established atherosclerosis [ 7 ].

These are clearly the pears with a preserved waist size, and they were recruited at random with two controls matched for age only. In their paper published in this edition of the Netherlands Heart Journal the authors describe a relation between the occurrence of a myocardial infarction MI in post-menopausal women and levels of sex hormones [ 1 ]. This story is confusing. Yet the beneficial effects of hormone replacement therapy were off set by the induction of thrombosis, likely in subjects who already had coronary artery disease [ 2 ]. Where we assumed that increased levels of female sex hormones were protective against the development of cardiovascular disease, our colleagues Mei Dong et al. The question is to what extent do the sex hormone levels contribute independently? In conclusion, whether in this study the observed elevated oestrogens were instrumental in causing the infarction or epiphenomenal to an adrenal stress response and increased peripheral sex hormone conversion potential still remains to be answered. They also had a lower body mass index BMI. Appelman, Email: Can we think of a possible mechanism by which it may cause MI? An important restriction of the paper by Dong et al. With only one measurement reported the temporal changes in sex hormone levels are not available. Not only the distribution of the fat tissue is crucial, also the other risk factors should be checked and treated, especially diabetes and hypertension. Appelman C. It has been reported that sex hormone levels are positively related to the total amount of fat tissue, with an inverse relation to sex hormone binding globulin [ 4 ]. The sex hormone story in relation to cardiovascular disease is always good for a surprise. So it is not unlikely that in the current study the observed higher oestrogen levels are an association with known risk factors that lead to MI rather than being causative. Based on these observations studies were initiated to supply sex hormones in order to postpone the onset of atherosclerosis. Appelman Find articles by Y. In men higher testosterone levels are associated with a reduced prevalence of metabolic syndrome and an elevated prevalence in women [ 9 ]. There are no indications that long-term administration of androgens to women, as occurs in the treatment of female-to-male transsexuals, is associated with a substantial increase of cardiovascular risk factors [ 8 ]. These are all changes related to the postmenopausal status and it is well known that all these factors contribute to an increased risk for MI. From an epidemiological perspective it was shown that in women there is a relation between the onset of the menopause and the risk of MI. In their discussion the focus in literature is on the lowering of testosterone in males during stress and a lowering of oestrogens in females. In fact, in postmenopausal women androgen secretion originates from the ovarian hilus driven by high gonadotropins and the adrenal gland driven by adrenocorticotrophic hormone and the oestrogens come from peripheral conversion of these androgens.

They also had a lower body mass index BMI. So it is not unlikely that in the current study the observed higher oestrogen levels are an association with known risk factors that lead to MI rather than being causative. Where we assumed that increased levels of female sex hormones were protective against the development of cardiovascular disease, our colleagues Mei Dong et al. The control group had lower WHR and lower levels of sex hormones. In their paper published in this edition of the Netherlands Heart Journal the authors describe a relation between the occurrence of a myocardial infarction MI in post-menopausal women and levels of sex hormones [ 1 ]. However, recent publications might change this view, as a recent paper by Schierbeck from Denmark demonstrated that an early start of hormone replacement therapy seems to benefit and decreases future atherosclerotic events [ 3 ]. So clearly the groups are very different. Appelman Find articles by Y. Women with polycystic ovarian syndrome PCOS , an ovulation disorder associated with increased androgen levels, are more at risk to develop cardiovascular disease. Theoretically, these findings by Dong et al. These are all changes related to the postmenopausal status and it is well known that all these factors contribute to an increased risk for MI. Not only the distribution of the fat tissue is crucial, also the other risk factors should be checked and treated, especially diabetes and hypertension.

They also had a lower body mass index BMI. With only one measurement reported the temporal changes in sex hormone levels are not available. Based on these observations studies were initiated to supply sex hormones in order to postpone the onset of atherosclerosis.
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